Enterotoxaemia

Enterotoxaemia occurs when specific bacteria (Clostridium perfringens) normally present in the gut, proliferate and produce toxins that are absorbed.

Conditions that favour excessive proliferation of clostridial organisms include carbohydrate overload, acidosis, higher flow of proteins and sugars from the rumen into the small intestine and motility disturbances that slow the flow of ingesta.

C. perfringens proliferates and produces toxins in the small intestine when intake of carbohydrate is high and there is overflow from the rumen and abomasum into the intestine. The epsilon toxin produced by type D bacteria causes increased vascular permeability with subsequent oedema. Development of oedema in the brain is associated with neurological signs. The beta toxin produced by type C has more direct effects on the intestinal epithelium, causing severe necrotic enteritis.

Classic enterotoxaemia due to C. perfringens type D is more common in the export process than type C. It may affect sheep, goats and cattle, but is most commonly reported in sheep. In feedlot situations it is seen in young, unvaccinated animals that are rapidly switched to high grain diets. A chronic form of enterotoxaemia occurs occasionally with the development of focal symmetrical encephalomalacia (FSE).

The proliferation of C. perfringens type C produces a different toxin (beta toxin) that causes necrotic enteritis with a high fatality rate in young animals and less commonly clinical disease in adult sheep, goats and cattle.

Peracute and acute cases are more common in susceptible animals. These cases may be found dead or die rapidly after short episodes of excitement and convulsion, sometimes with opisthotonos (head arched back over the body). Affected animals may also vocalise (bleating), circle, head press, become recumbent and paddle or froth at the mouth. Profuse watery diarrhoea may also be seen (more commonly in goats than sheep).

Subacute and chronic cases also occur occasionally in sheep and goats. Chronically affected animals may deteriorate and die or may slowly recover.

Sheep that survive an initial acute insult appear to be likely to develop focal symmetrical encephalomalacia (FSE) due to chronic effects of toxins on the brain. Animals with FSE may show dullness, ataxia, incoordination, weakness and other neurological signs depending on the extent of damage, and progressive weight loss.

Goats may be less likely to show neurological signs in subacute and chronic cases and more likely to show signs of enteritis. Although they may also develop opisthotonos and convulsions shortly before death.

Diagnosis is typically made at necropsy. A full rumen and undigested feed in the lower intestines are evidence of overeating and should raise suspicions. Pulpy kidneys are an inconsistent finding and not specific to enterotoxaemia.

Sheep. If the necropsy interval is short, high levels of glucose are present in the urine and readily measured by dipstick (glucosuria may occur in ruminants that are stressed for any reason due to a low renal threshold for glucose). If necropsy is delayed, glucose is rapidly fermented by bacteria in urine and may not be elevated. The lungs are wet and heavy. The membranes on the surface of the heart (epicardium) and lining the heart chambers (endocardium) may be streaked with haemorrhages, and the pericardium often contains increased clear fluid with floating strands of protein.

Goats. In goats, post-mortem appearances resemble those in sheep but may be restricted to the gut, in particular, the coiled colon. The lumen of the coiled colon is empty, the wall thickened and contracted, and the mucosa is rough and eroded.

Specimens for laboratory confirmation include smears for bacteriology from inflamed and adjacent non-inflamed sites along the intestinal mucosa; intestinal content (40mL) especially yellow creamy material, for toxicology; and the whole brain and sections of liver and kidney in buffered formalin for histology.